You Know What They Say About a Beetle With a Really Big Horn?
July 29, 2012 § Leave a comment
He must have had some really high insulin levels when he was growing up!
No, seriously. That’s what they say. They, in this case, being a quintet of biologists from the University of Montana (among other places), who’ve come out with a new study detailing the likely molecular underpinnings of the extravagantly long, wildly varied horn of the male Japanese rhinoceros beetle.
Yep, there it is: the giant branch coming off his face. It’s a terribly useful tool for a beetle, perfect for knocking male competitors out of the way during a fight for a lady beetles—which naturally makes bigger all the better. Unfortunately for the poorly endowed, the size of the horn is entirely determined by the growing conditions the beetle endured as a grub. Good food and low stress make for a huge, manly horn that can, in the best of times, grow up to nearly the length of the beetle. Poor nutrition, infection, or bad genes leads to a sad little stump that won’t be much use against a bigger male.
Now, the operating factor in all of this is insulin and the insulin-like growth factor (IGF) system. That’s also the molecular key that determines how big the beetle becomes as a whole. You’ve actually got the same thing; it’s what made you grow while you were on the up and up, and ditto me, my cat, fish, reptiles, crustaceans, and so on. More food leads to more insulin, which powers the engine that leads to more growth, and vice versa. It’s one of the oldest, most conserved systems in the evolutionary playbook.
But here’s a question: given that the size of the beetle and his horn are both being driven by the same conditions and the same insulin levels, how is the horn able to grow to such massive sizes compared to the rest of the beetle? Because seriously, the beetle’s food isn’t actually going straight to his horn any more than a piece of cake is literally going straight to my hips.
As the Montana crew figured it, given insulin’s dominant role in growth, there might be some sort of horn-only hypersensitivity to the insulin signaling. To test the theory, they reared a collection of male grubs, waited until after the beetles’ bodies had fully developed, but before the genitals, wings, and horns had finished, then they tossed a molecular monkey wrench into the insulin system, knocking it down for 48 hours.
When all was said and done, the wings—which typically in proportion to the rest of the body—were stunted by about two percent compared to normal beetle proportions. The horns on the other hand, had been hugely cut down and were smaller by a full 16 percent. Just imagine if the disruption had screwed signaling the other way and increased growth instead of knocking it down. You’d have horns growing at eight times the rate of other body parts (which actually, is probably exactly what happens). Thank the heavens that evolution had the good sense to make the genitals effectively immune from this—their size wasn’t affected at all by the tweak, for which I will assume female beetles everywhere are probably grateful.
But wait! There’s more! See, the main tool by which an organism usually becomes more or less sensitive to something is in the chemical receptors. Depending on its goal, the body can throw in more or fewer receptors to tweak sensitivity. (Cocaine addicts for instance, have fewer dopamine receptors in their brains because they’ve overwhelmed the system with dopamine-like cocaine and their bodies are desperately trying to tamp things down.) This is neuroscience 101, and yet it did not hold true here. Before the experimenters’ intervention kicked in, the team had checked insulin receptor levels and found them to be roughly equivalent between the wings and horns.
“The textbook is assumption is that if your tissue is going to be sensitive to hormones, it’s going to be by the receptor,” Emlen says. “And that’s how we walked into it, too. It’s why we picked that gene first. But biology doesn’t always work the way you think.”
Something else is therefore at play—something new and probably awesome, and if you can bear with me, I’m going to just go ahead and explore the sexual organs of fruit flies while I give you an alternative. See, this beetle work builds directly on a paper that came out of Michigan State University, in which researchers tackled another example of disproportionate growth, this time in fruit flies. Just like rhino beetles, nutrition and insulin during growth determine the body size of an adult fly. However both large flies and small ones—even those fed on near starvation diets—are more or less equally well-endowed, genitally speaking (although it’s possible smaller flies look proportionally more impressive naked). Once again, this mechanism was clearly not tied to direct differences in the insulin receptor of the different organs. But it was tied to something else, specifically to much lower levels in the genitals of a gene called FOXO, which typically acts within the insulin cascade as the brakes on growth when food is scarce. That genital-only difference in downstream stopping power was what desensitized the organs from insulin’s rises and falls.
“That was a really important precedent,” Emlen says. “It was groundbreaking in setting the stage for us in saying that traits can change. You can have changes that affect one structure that don’t necessarily have to affect everything else.” But whether a similar process operates the other way wasn’t testable in flies—they simply don’t have any massively overgrown, potentially hypersensitive ornaments to examine. Hence the beetles.
Based on Emlen’s study, hypersensitivity via … well, via something in the insulin pathway clearly is going on in rhino beetles, but now the question is what. It might be FOXO, but it might not. Emlen’s lab is already working on it, both in those beetles and in as many others he can get his hands on.”We’re going to know—ask me in six months,” he says.
The combined work has the potential to spill over into disease research: aging issues, some types of cancers, and certainly diabetes hang on issues of growth or insulin sensitivity. But it also sets the stage for evolutionary researchers. The world is filled with examples of wildly dimorphic weaponry: deer antlers, the fiddler crab’s claw. And everybody has a theory for why these evolved—ladies love them, they’re great for fighting, or they’re a way of showing that the guy’s got such fabulous genetic material that he physically is capable of dragging around that ungainly pile of peacock feathers. “Most evolutionary biologists working in this area have treated organisms as ‘black boxes’ however, and not really looked at the mechanisms, so until now, we have had very little idea as to how it comes about,” says Rob Knell, a researcher at the Queen Mary University of London who also explores the evolution of sexual ornamentation and weaponry and was unassociated with this study. “I’m pretty excited about this and looking forward to finding out how general this sort of mechanism is.”
Hey, by the way, you know what they say about a guy with really big feet?
Yeah, that’s not true.
Emlen DJ, Warren IA, Johns A, et al. A Mechanism of Extreme Growth and Reliable Signaling in Sexually Selected Ornaments and Weapons. Published online 26 July 2012 (DOI:10.1126/science.1224286).